Atrial fibrillation together with atrial flutter is the most commonly sustained arrhythmia found in clinical practice. Although there has been an increased awareness in the last several years of the potentially serious clinical consequences of both arrhythmias, their basic electrophysiological mechanisms and optimal management strategies only recently have been understood. Atrial fibrillation (AF) involves rapid and chaotic beating of the individual fibers of the heart muscle such that synchronous contraction is not maintained. This inevitably results in that part of the heart ceasing to pump blood, which in turn can lead to embolic stroke. Atrial fibrillation is characterized by the presence of multiple reentrant circuits that may be active simultaneously, precluding the synchronous activation of enough atrial myocardium to generate an identifiable p wave or coordinated atrial contraction. Either a sinus impulse or a stable atrial flutter reentrant circuit (flutter wave) may degenerate into the multiple reentrant circuits (multiple wavelets) characteristic of atrial fibrillation, (Cox et al., J. Thoracic. Cardiovas. Surg. 101: 402-405 1991).
Atrial fibrillation currently afflicts over three million persons in the United States. (Cox et al., J. Thoracic. Cardiovas. Surg. 101: 402-405 1991). It is the most commonly sustained arrhythmia, increasing progressively in prevalence with advancing age, and occurring in 2%-4% of the population over the age of 60. Atrial fibrillation is associated with atherosclerosis, chronic rheumatic heart disease, hypertensive heart disease and stroke.
Our current understanding is that atrial fibrillation (AF) is initiated most often by a focal trigger from the orifice of or from within one of the pulmonary veins. Though mapping and ablation of these triggers appears to be curative in most patients with paroxysmal AF, there are a number of limitations to ablating focal triggers via mapping and ablating the earliest site of activation with a “point” radiofrequency lesion. One way to circumvent these limitations is to determine precisely the point of earliest activation. Once the point of earliest activation is identified, a lesion can be generated to electrically isolate the trigger. By electrically isolating one or more of the triggers in the pulmonary veins from the left atrium with a lesion, firing from within those veins would be unable to reach the body of the atrium, and thus could not trigger atrial fibrillation.
There are several catheter-based therapeutic modalities currently being used for the treatment of atrial fibrillation. However, there is still recurrence of atrial fibrillation after catheter ablation. It is difficult to predict the long-term success or recurrence. In the attempt to increase the long-term success rate, several modified therapies are proposed and practiced, for example, adding one or more linear lesions in the left atrium, the right atrium, or both, and creating a larger area of lesions that surround the left atrial tissue and junction of the pulmonary veins. However, the mechanism of this kind of approach is not clear and may in fact be destructive to mechanical function of the heart in the long term. Therefore, what is needed in the art is a more predictive approach and tools therefor that are able to evaluate the substrate of atrial arrhythmias, which include atrial fibrillation, and to provide direction for future intervention in addition to the elimination of the arrhythmic foci. Furthermore, what is needed in the art is a predictive parameter that can indicate long-term success likelihood to the electrophysiologist.
U.S. Pat. No. 6,081,746 discusses AFCL in the context of pacing the heart. This patent recognizes that the AFCL varies with regions of the heart, but suggests that the AFCL value sensed at the Bachmann's Bundle is adequate for use in pacing despite variations that may exist through the heart tissue.
Atrial cycle length is an important intrinsic property of atrial tissue. It provides a characterization of the substrate of the atrial tissue of AF patients. However, due to the chaotic nature of waveforms during AF, it is difficult to interpret cycle length of atrial tissue on a beat-by-beat basis. Rather, an average atrial fibrillation cycle length (“AFCL”) has been manually calculated by electrophysiologists to determine the vulnerability of atrial tissue to AF trigger. It also is used to aid operators in deciding whether or not to create any or any additional lesions using an ablation catheter or other instrument. To determine the Atrial Fibrillation Cycle Length (AFCL), EP physicians have used a conventional catheter by moving the catheter within and around the atrium to survey the targeted atrial tissue; the AFCL is manually calculated by taking the total cycle length at a certain period, e.g. 2 seconds, divided by the total peaks of atrial activation. Electrocardiograms are analyzed carefully to reject low-amplitude potentials and to detect double potentials associated with block, correlation with the surface ECG was used to eliminate the ventricular electrocardiogram. The procedure is subjective, tedious and is time-consuming and has not provided a convenient, rapid, and repeatable approach to evaluating and utilizing AFCL determinations. The present invention addresses one or more of these and other deficiencies in the prior art.